研究者詳細 - 鈴木　弘美

論文 - 鈴木　弘美

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LC-MS/MS imaging with thermal film-based laser microdissection. 査読有り国際共著国際誌

Oya M, Suzuki H, Anas ARJ, Oishi K, Ono K, Yamaguchi S, Eguchi M, Sawada M

Analytical and bioanalytical chemistry 410 巻 ( 2 ) 頁： 491 - 499 2018年1月

Signal Sequence-Dependent Orientation of Signal Peptide Fragments to Exosomes. 査読有り

Ono K, Niwa M, Suzuki H, Kobayashi NB, Yoshida T, Sawada M

International Journal of Molecular Sciences 23 巻 ( 6 ) 頁： 3137 2022年3月

記述言語：英語掲載種別：研究論文（学術雑誌）

Signal peptides (SPs) not only mediate targeting to the endoplasmic reticulum (ER) but also play important roles as biomarkers and substances with physiological activity in extracellular fluids including blood. SPs are thought to be degraded intracellularly, making it unclear how they are transported from the ER to the extracellular fluid. In a recent study, we showed that a C-terminal fragment of the SP of a type I membrane protein, amyloid precursor protein (APP), was secreted into the extracellular fluid via exosomes using transformed HEK293 cells expressing APP SP flanking a reporter protein. In the present study, we demonstrate that a N-terminal fragment of the SP from a type II membrane protein, human placental secreted alkaline phosphatase (SEAP), is contained in exosomes and secreted into the extracellular fluid using HEK-Blue hTLR3 cells, which express both a human toll-like receptor 3 gene and an inducible SEAP reporter gene. When HEK-Blue hTLR3 cells were stimulated with a TLR3 ligand, a N-terminal fragment of SEAP SP in exosomes was increased in parallel with SEAP secretion in a concentration-dependent manner. These results indicated that SP fragments are exosomal components. In addition, migrating SP fragments were determined by characteristics of the signal–anchor sequence of membrane proteins. Furthermore, we found that SP fragments could bind to calmodulin (CALM), which is a cytosolic protein and also a component of exosomes, suggesting its involvement in the transportation of SP fragments from the endoplasmic reticulum to exosomes.

DOI： 10.3390/ijms23063137

その他リンク： https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8950404/

Secretion of signal peptides via extracellular vesicles 査読有り国際誌

Ono K, Niwa M, Suzuki H, Kobayashi NB, Yoshida T, Sawada M.

Biochem Biophys Res Commun . 560 巻頁： 21 - 26 2021年5月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Elsevier

Signal peptides (SPs) consist of short peptide sequences present at the N-terminal of newly synthesizing proteins and act as a zip code for the translocation of the proteins to the endoplasmic reticulum (ER). It was thought that the SPs are intracellularly degraded after translocation to the ER; however, recent studies showed cleaved SPs have diverse roles for controlling cell functions in auto- and/or intercellular manners. In addition, it still remains obscure how SP fragments translocate away from the site where they are produced. Extracellular vesicles (EV) are important for intercellular communication and can transport functional molecules to specific cells. In this study, we show that SPs are involved in EV from T-REx AspALP cells that were transfected with a human APP SP-inducible expression vector. There was no difference in the average particle size or particle concentration of EV collected from T-REx AspALP cells and T-REx Mock cells. When the SP content in the EV was examined by mass spectrometry, the C-terminal fragment of APP SP was identified in the exosomes (SEV) of T-REx AspALP cells. In our preparation of SEV fractions, no ER-specific proteins were detected; therefore, SPs may be included in SEV but not in the debris of degraded ER. This is the first indication that SPs are secreted from cells via EV.

DOI： 10.1016/j.bbrc.2021.04.073.

Peripheral benzodiazepine receptor/18 kDa translocator protein positron emission tomography imaging in a rat model of acute brain injury 査読有り国際共著

Nomura M, Toyama H, Suzuki H, Yamada T, Hatano K, Alan A Wilson, Ito K, Sawada M

Ann Null Med. 35 巻 ( 1 ) 頁： 8 - 16 2021年1月

Distribution of Signal Peptides in Microvesicles from Activated Macrophage Cells. 招待有り査読有り

Ono K, Sato J, Suzuki H, Sawada M

International journal of molecular sciences 24 巻 ( 15 ) 2023年7月

Calmodulin as a Key Regulator of Exosomal Signal Peptides. 招待有り査読有り国際誌

Ono K, Niwa M, Suzuki H, Kobayashi NB, Yoshida T, Sawada M

Cells 12 巻 ( 1 ) 頁： 158 2022年12月

Inhibition of cellular inflammatory mediator production and amelioration of learning deficit in flies by deep sea Aspergillus-derived cyclopenin. 査読有り国際共著

Wang L, Li M, Lin Y, Du S, Liu Z, Ju J, Suzuki H, Sawada M, Umezawa K

The Journal of antibiotics 73 巻 ( 9 ) 頁： 622 - 629 2020年9月

記述言語：英語掲載種別：研究論文（学術雑誌）

In the course of screening lipopolysaccharide (LPS)-induced nitric oxide (NO) production inhibitors, two related benzodiazepine derivatives, cyclopenol and cyclopenin, were isolated from the extract of a deep marine-derived fungal strain, Aspergillus sp. SCSIOW2. Cyclopenol and cyclopenin inhibited the LPS-induced formation of NO and secretion of IL-6 in RAW264.7 cells at nontoxic concentrations. In terms of the mechanism underlying these effects, cyclopenol and cyclopenin were found to inhibit the upstream signal of NF-κB activation. These compounds also inhibited the expression of IL-1β, IL-6, and inducible nitric oxide synthase (iNOS) in mouse microglia cells, macrophages in the brain. In relation to the cause of Alzheimer’s disease, amyloid-β-peptide is known to induce inflammation in the brain. Therefore, the present study investigated the ameliorative effects of these inhibitors on an in vivo Alzheimer’s model using flies. Learning deficits were induced by the overexpression of amyloid-β42 in flies, and cyclopenin but not cyclopenol was found to rescue learning impairment. Therefore, novel anti-inflammatory activities of cyclopenin were identified, which may be useful as a candidate of anti-inflammatory agents for neurodegenerative diseases.

DOI： 10.1038/s41429-020-0302-9

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PubMed

Dipeptidyl peptidase-4 inhibition prevents nonalcoholic steatohepatitis-associated liver fibrosis and tumor development in mice independently of its anti-diabetic effects 査読有り国際共著

Mitsuhiro Kawakubo, Miyako Tanaka, Kozue Ochi, Akiko Watanabe, Marie Saka-Tanaka, Yohei Kanamori, Naoki Yoshioka, Satoko Yamashita, Moritaka Goto, Michiko Itoh, Ibuki Shirakawa, Sayaka Kanai, Hiromi Suzuki, Makoto Sawada, Ayaka Ito, Masatoshi Ishigami, Mitsuhiro Fujishiro, Hiroshi Arima, Yoshihiro Ogawa, Takayoshi Suganami

Science Report 10 巻 ( 1 ) 頁： 983 2020年1月

記述言語：英語掲載種別：研究論文（学術雑誌）

Nonalcoholic steatohepatitis (NASH) is a hepatic phenotype of the metabolic syndrome, and increases the risk of cirrhosis and hepatocellular carcinoma (HCC). Although increasing evidence points to the therapeutic implications of certain types of anti-diabetic agents in NASH, it remains to be elucidated whether their effects on NASH are independent of their effects on diabetes. Genetically obese melanocortin 4 receptor-deficient (MC4R-KO) mice fed Western diet are a murine model that sequentially develops hepatic steatosis, NASH, and HCC in the presence of obesity and insulin resistance. In this study, we investigated the effect of the dipeptidyl peptidase-4 (DPP-4) inhibitor anagliptin on NASH and HCC development in MC4R-KO mice. Anagliptin treatment effectively prevented inflammation, fibrosis, and carcinogenesis in the liver of MC4R-KO mice. Interestingly, anagliptin only marginally affected body weight, systemic glucose and lipid metabolism, and hepatic steatosis. Histological data and gene expression analysis suggest that anagliptin treatment targets macrophage activation in the liver during the progression from simple steatosis to NASH. As a molecular mechanism underlying anagliptin action, we showed that glucagon-like peptide-1 suppressed proinflammatory and profibrotic phenotypes of macrophages in vitro. This study highlights the glucose metabolism-independent effects of anagliptin on NASH and HCC development.

DOI： 10.1038/s41598-020-57935-6

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Novel Oxindole-Curcumin Hybrid Compound for Antioxidative Stress and Neuroprotection 査読有り

Yoko Hirata, Yuki Ito, Madoka Takashima, Kazuya Yagyu, Kentaro Oh-Hashi, Hiromi Suzuki, Kenji Ono, Kyoji Furuta, Makoto Sawada

ACS Chem Neurosci . 11 巻 ( 1 ) 頁： 76-85 2020年1月

記述言語：英語掲載種別：研究論文（学術雑誌）

Oxidative stress plays an important role in the pathogenesis of Parkinson's disease and other neurodegenerative disorders. The oxindole compound GIF-2165X-G1 is a hybrid molecule composed of the oxindole skeleton of the neuroprotective compound GIF-0726-r and the polyphenolic skeleton of the antioxidant curcumin. We previously reported that novel oxindole derivatives such as GIF-0726-r and GIF-2165X-G1 prevent endogenous oxidative stress-induced cell death in mouse hippocampal HT22 cells. In this study, we present a detailed investigation of the effect of GIF-2165X-G1 on endogenous oxidative stress in HT22 cells in comparison with GIF-0726-r and curcumin. GIF-2165X-G1 exhibited more potent neuroprotective activity than GIF-0726-r or curcumin and had less cytotoxicity than that observed with curcumin. Both GIF-0726-r and GIF-2165X-G1 were found to have ferrous ion chelating activity similar to that exhibited by curcumin. GIF-2165 X-G1 and curcumin induced comparable antioxidant response element transcriptional activity. Although the induction of heme oxygenase-1, an antioxidant response element-regulated gene product, was much stronger in curcumin-treated cells than in GIF-2165X-G1-treated cells, it turned out that the induction of heme oxygenase-1 is dispensable for neuroprotection. These results demonstrate that the introduction of the polyphenol skeleton of curcumin to the oxindole GIF-0726-r improves neuroprotective features. Furthermore, intrastriatal injection of GIF-2165X-G1 alleviated apomorphine-induced rotation and prevented dopaminergic neuronal loss in a 6-hydroxydopamine mouse model of Parkinson's diseases. Collectively, our novel findings indicate that the novel oxindole compound GIF-2165X-G1 serves to delay the progression of Parkinson's disease by suppressing oxidative stress.

DOI： 10.1021/acschemneuro.9b00619.

Novel oxindole derivatives prevent oxidative stress-induced cell death in mouse hippocampal HT22 cells. 査読有り

Hirata Y, Yamada C, Ito Y, Yamamoto S, Nagase H, Oh-Hashi K, Kiuchi K, Suzuki H, Sawada M, Furuta K

Neuropharmacology 135 巻頁： 242-252 2018年3月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Science Direct

The current medical and surgical therapies for neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease offer symptomatic relief but do not provide a cure. Thus, small synthetic compounds that protect neuronal cells from degeneration are critically needed to prevent and treat these. Oxidative stress has been implicated in various pathophysiological conditions, including neurodegenerative diseases. In a search for neuroprotective agents against oxidative stress using the murine hippocampal HT22 cell line, we found a novel oxindole compound, GIF-0726-r, which prevented oxidative stress-induced cell death, including glutamate-induced oxytosis and erastin-induced ferroptosis. This compound also exerted a protective effect on tunicamycin-induced ER stress to a lesser extent but had no effect on campthothecin-, etoposide- or staurosporine-induced apoptosis. In addition, GIF-0726-r was also found to be effective after the occurrence of oxidative stress. GIF-0726-r was capable of inhibiting reactive oxygen species accumulation and Ca2+ influx, a presumed executor in cell death, and was capable of activating the antioxidant response element, which is a cis-acting regulatory element in promoter regions of several genes encoding phase II detoxification enzymes and antioxidant proteins. These results suggest that GIF-0726-r is a low-molecular-weight compound that prevents neuronal cell death through attenuation of oxidative stress. Among the more than 200 derivatives of the GIF-0726-r synthesized, we identified the 11 most potent activators of the antioxidant response element and characterized their neuroprotective activity in HT22 cells.

DOI： 10.1016/j.neuropharm.2018.03.015

PubMed

Inducible nitric oxide synthase during the late phase of sepsis is associated with hypothermia and immune cell migration. 査読有り

Takatani Y, Ono K, Suzuki H, Inaba M, Sawada M, Matsuda N

Laboratory investigation 98 巻 ( 5 ) 頁： 629 - 639 2018年2月

記述言語：英語掲載種別：研究論文（学術雑誌）

Hypothermia is a significant sign of sepsis, which is associated with poor prognosis, but few mechanisms underlying the regulation of hypothermia are known. Inducible nitric oxide synthase (iNOS) is a key inflammatory mediator of sepsis. However, the therapeutic benefit of iNOS inhibition in sepsis is still controversial, and requires elucidation in an accurate model system. In this study, wild-type (WT) mice showed temperature drops in a biphasic manner at the early and late phase of sepsis, and all mice died within 48 h of sepsis. In contrast, iNOS-knockout (KO) mice never showed the second temperature drop and exhibited improved mortality. Plasma nitric oxide (NO) levels of WT mice increased in the late phase of sepsis and correlated to hypothermia. The results indicate that iNOS-derived NO during the late phase of sepsis caused vasodilation-induced hypothermia and a lethal hypodynamic state. The expression of the iNOS mRNA was high in the lung of WT mice with sepsis, which reflects the pathology of acute respiratory distress syndrome (ARDS). We obtained the results in a modified keyhole-type cecal ligation and puncture model of septic shock induced by minimally invasive surgery. In this accurate and reproducible model system, we transplanted the bone marrow cells of GFP transgenic mice into WT and iNOS-KO mice, and evaluated the role of increased pulmonary iNOS expression in cell migration during the late phase of sepsis. We also investigated the quantity and type of bone marrow-derived cells (BMDCs) in the lung. The number of BMDCs in the lung of iNOS-KO mice was less than that in the lung of WT mice. The major BMDCs populations were CD11b-positive, iNOS-negative cells in WT mice, and Gr-1-positive cells in iNOS-KO mice that expressed iNOS. These results suggest that sustained hypothermia may be a beneficial guide for future iNOS-targeted therapy of sepsis, and that iNOS modulated the migratory efficiency and cell type of BMDCs in septic ARDS.

DOI： 10.1038/s41374-018-0021-z

PubMed

Visualization of Arc promoter-driven neuronal activity by magnetic resonance imaging 査読有り

Qi Wu, Kenji Ono, Hiromi Suzuki, Megumi Eguchi, Shun Yamaguchi, Makoto Sawada

Neuroscience Letters 666 巻頁： 92 - 97 2018年2月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Elsevier Ireland Ltd

Visualization of direct neuronal activity to understand brain function is one of the most important challenges in neuroscience. We have previously demonstrated that in vivo and in vitro gene expression of the ferritin reporter system could be detected by magnetic resonance imaging (MRI). In addition, increased neuronal activity induces Arc, an immediate early gene, and insertion of a destabilized fluorescent reporter dVenus under Arc promoter control has been used for monitoring neuronal activities in the brain by optical imaging. In this study, to visualize Arc promoter-driven neuronal activities directly, we generated transgenic mice and cell lines that express a destabilized fusion reporter ferritin-mKate2 under Arc promoter control. When transgenic mice and cell lines were treated with pilocarpine, a non-selective muscarinic agonist, an increase in T2-weighted image signal was successfully found in neuronal cells. There was a difference in peak time between MRI and fluorescence imaging, which might result from the binding process of iron with ferritin. Visualization of Arc promoter-driven neuronal activity is essential to understand neural mechanisms underlying cognitive processes and complex behaviors, and could be a useful tool for therapeutic approaches in the brain by MRI.

DOI： 10.1016/j.neulet.2017.12.041

Web of Science

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PubMed

Optogenetic control of cell differentiation in channelrhodopsin-2-expressing OS3, a bipotential glial progenitor cell line

Ono K, Suzuki H, Yamamoto R, Sahashi H, Takido Y, Sawada M.

Neurochemistry International 104 巻頁： 49-63 2017年3月

Radiosynthesis and in vivo evaluation of two imidazopyridineacetamides, [(11)C]CB184 and [ (11)C]CB190, as a PET tracer for 18 kDa translocator protein: direct comparison with [ (11)C](R)-PK11195. 招待有り査読有り

Hatano K, Sekimata K, Yamada T, Abe J, Ito K, Ogawa M, Magata Y, Toyohara J, Ishiwata K, Biggio G, Serra M, Laquintana V, Denora N, Latrofa A, Trapani G, Liso G, Suzuki H, Sawada M, Nomura M, Toyama H

Annals of nuclear medicine 29 巻 ( 4 ) 頁： 325 - 35 2015年5月

Protective effect of INI-0602, a gap junction inhibitor, on dopaminergic neurodegeneration of mice with unilateral 6-hydroxydopamine injection

SUZUKI Hiromi,ONO Kenji,SAWADA Makoto

Journal of Neural Transmission 121 巻 ( 11 ) 頁： 1349-1355 2014年11月

Glutamate release from astrocyte cell-line GL261 via alterations in the intracellular ion environment. 査読有り

Ono K, Suzuki H, Higa M, Tabata K, Sawada M

Journal of neural transmission (Vienna, Austria : 1996) 121 巻 ( 3 ) 頁： 245 - 57 2014年

Detection of cytotoxic activation of microglia in a rat neuroinflammation model using a novel translocator protein ligand, [18F]FEPPA 招待有り査読有り

Nomura, M; Toyama, H; Suzuki, H; Yamada, T; Ota, S; Ichise, M; Wilson, A; Sawada, M; Ito, K; Hatano, K

JOURNAL OF NUCLEAR MEDICINE 53 巻 2012年5月

Detection of cytotoxic activation of microglia in a rat neuroinflammation model using a novel translocator protein ligand, [18F]FEPPA 査読有り

Nomura,M, Toyama,H, Suzuki,H, Yamada,T, Ota,S, Ichise,M, Wilson,AA, Sawada,M, Ito,K, Hatano,K

J Nucl Med 53(Supplement 1) 巻頁： 1884 2012年

New fluorescent probes targeting the mitochondrial-located translocator protein 18 kDa (TSPO) as activated microglia imaging agents. 査読有り

DENORA N, LAQUINTANA V, TRAPANI A, SUZUKI H, SAWADA M, TRAPANI G

Pharmaceutical Research 28 巻 ( 11 ) 頁： 2820-2832 2011年11月

New Fluorescent Probes Targeting the Mitochondrial-Located Translocator Protein 18 kDa (TSPO) as Activated Microglia Imaging Agents 査読有り

Denora, N; Laquintana, V; Trapani, A; Suzuki, H; Sawada, M; Trapani, G

PHARMACEUTICAL RESEARCH 28 巻 ( 11 ) 頁： 2820 - 2832 2011年11月

Time-dependent changes in proinflammatory and neurotrophic responses of microglia and astrocytes in a rat model of osmotic demyelination syndrome. 査読有り

IWAMA S, SUGIMURA Y, SUZUKI H, SUZUKI H, MURASE T, OZAKI N, NAGASAKI H, ARIMA H, MURATA Y, SAWADA M, OISO Y

Glia 59 巻 ( 3 ) 頁： 452-462 2011年3月

Time-Dependent Changes in Proinflammatory and Neurotrophic Responses of Microglia and Astrocytes in a Rat Model of Osmotic Demyelination Syndrome 査読有り

Iwama, S; Sugimura, Y; Suzuki, H; Suzuki, H; Murase, T; Ozaki, N; Nagasaki, H; Arima, H; Murata, Y; Sawada, M; Oiso, Y

GLIA 59 巻 ( 3 ) 頁： 452 - 462 2011年3月

Pathway analysis of single-microglia gene-expression profiles reveals the new molecular targets of minocycline treatment 招待有り査読有り

Suzuki Haruyuki, Sugimura Yoshihisa, Iwama Shintaro, Suzuki Hiromi, Takagi Hiroshi, Kiyota Atsushi, Fukuoka Kazuki, Sawada Makoto, Oiso Yutaka

NEUROSCIENCE RESEARCH 71 巻頁： E223 - E223 2011年

ミクログリアによるBBB非崩壊型の脳へのターゲティングDDS 招待有り査読有り

澤田誠, 鈴木弘美, 小野健治

薬剤学 71 巻 ( 5 ) 頁： 259 - 267 2011年

Visualization of iNOS gene expression from activated cells in magnetic resonance imaging 招待有り査読有り国際誌

Ono, K; Tabata, K; Suzuki, H; Sawada, M

NEUROSCIENCE RESEARCH 71 巻頁： E96 - E96 2011年

Minocycline Prevents Osmotic Demyelination Syndrome by Inhibiting the Activation of Microglia 招待有り査読有り

Suzuki Haruyuki, Sugimura Yoshihisa, Iwama Shintaro, Suzuki Hiromi, Nobuaki Ozaki, Nagasaki Hiroshi, Arima Hiroshi, Sawada Makoto, Oiso Yutaka

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY 21 巻 ( 12 ) 頁： 2090 - 2098 2010年12月

Electrosprayed Synthesis of Red-Blood-Cell-Like Particles with Dual Modality for Magnetic Resonance and Fluorescence Imaging 査読有り

Hayashi, K; Ono, K; Suzuki, H; Sawada, M; Moriya, M; Sakamoto, W; Yogo, T

SMALL 6 巻 ( 21 ) 頁： 2384 - 2391 2010年11月

Correlation between FEPPA uptake and microglia activation in 6-OHDA injured rat brain 招待有り査読有り

Hatano, K; Yamada, T; Toyama, H; Kudo, G; Nomura, M; Suzuki, H; Ichise, M; Wilson, AA; Sawada, M; Kato, T; Ito, K

NEUROIMAGE 52 巻頁： S138 - S138 2010年8月

High-frequency, magnetic-field-responsive drug release from magnetic nanoparticle/organic hybrid based on hyperthermic effect.

HAYASHI K, ONO K, SUZUKI H, SAWADA M, MORIYA M, SAKAMOTO W, YOGO T

ACS applied materials & interfaces 2 巻 ( 7 ) 頁： 1903-1911 2010年7月

One-Pot Biofunctionalization of Magnetic Nanoparticles via Thiol-Ene Click Reaction for Magnetic Hyperthermia and Magnetic Resonance Imaging 招待有り査読有り

Hayashi Koichiro, Ono Kenji, Suzuki Hiromi, Sawada Makoto, Moriya Makoto, Sakamoto Wataru, Yogo Toshinobu

CHEMISTRY OF MATERIALS 22 巻 ( 12 ) 頁： 3768 - 3772 2010年6月

Delayed neural damage is induced by iNOS-expressing microglia in a brain injury model 招待有り査読有り

Ono, K; Suzuki, H; Sawada, M

NEUROSCIENCE LETTERS 473 巻 ( 2 ) 頁： 146 - 150 2010年4月

Two activated stages of microglia and PET imaging of peripheral benzodiazepine receptors with [^<11>C]PK11195 in rats 招待有り査読有り

ITO Fumitaka, TOYAMA Hiroshi, KUDO Gen, SUZUKI Hiromi, HATANO Kentaro, ICHISE Masanori, KATADA Kazuhiro, ITO Kengo, SAWADA Makoto

Annals of nuclear medicine 24 巻 ( 3 ) 頁： 163 - 169 2010年4月

Delayed neural damage is induced by iNOS-expressing microglia in a brain injury model 査読有り

ONO Kenji, SUZUKI Hiromi, SAWADA Makoto

Neuroscience Letters 473 巻 ( 2 ) 頁： 146-150 2010年4月

Two activated stages of microglia and PET imaging of peripheral benzodiazepine receptors with [C-11]PK11195 in rats 招待有り査読有り

Ito Fumitaka, Toyama Hiroshi, Kudo Gen, Suzuki Hiromi, Hatano Kentaro, Ichise Masanori, Katada Kazuhiro, Ito Kengo, Sawada Makoto

ANNALS OF NUCLEAR MEDICINE 24 巻 ( 3 ) 頁： 163 - 169 2010年4月

Comparison of the neurological sequelae after rapid correction of hyponatremia between by vasopressin receptor antagonist mozavaptan (OPC-31260) and by hypertonic saline in rats 招待有り査読有り

Suzuki, H; Sugimura, Y; Iwama, S; Nagasaki, H; Arima, H; Oiso, Y

ENDOCRINE JOURNAL 57 巻頁： S531 - S531 2010年3月

Neuroprotective and Neurotoxic Phenotypes of Activated Microglia in Neonatal Mice with Respective MPTP- and Ethanol-Induced Brain Injury. 査読有り

Sawada H, Suzuki H, Nagatsu T, Sawada M.

Neuro-degenerative Diseases 7 巻 ( 1-3 ) 頁： 64-67 2010年2月

Minocycline prevents osmotic demyelination syndrome by inhibiting the activation of microglia. 査読有り

SUZUKI H, SUGIMURA Y, IWAMA S, SUZUKI H, OZAKI N, NAGASAKI H, ARIMA H, SAWADA M, OISO Y.

Journal of the American Society of Nephrology 21 巻 ( 12 ) 頁： 2090-2098 2010年

Control of activation in ChR2-expressing astrocytes by blue light exposure 招待有り査読有り

Ono, K; Higa, M; Tabata, K; Suzuki, H; Sawada, M

NEUROSCIENCE RESEARCH 68 巻頁： E57 - E57 2010年

Neuroprotective and neurotoxic phenotypes of activated microglia in neonatal mice with respective MPTP- and ethanol-induced brain injury. 招待有り査読有り

Sawada H, Suzuki H, Nagatsu T, Sawada M

Neuro-degenerative diseases 7 巻 ( 1-3 ) 頁： 64 - 7 2010年

Gene expression profiling of microglia from the demyelinative lesions in osmotic demyelination syndrome rats 招待有り査読有り

Sugimura, Y; Suzuki, H; Iwama, S; Suzuki, H; Kiyota, A; Sawada, M; Oiso, Y

NEUROSCIENCE RESEARCH 68 巻頁： E199 - E199 2010年

小動物における定量的画像解析招待有り査読有り

外山宏, 旗野健太郎, 鈴木弘美, 工藤元, 野村昌彦, 山田貴史, 木村裕一, 市瀬正則, 澤田誠

脳循環代謝 21 巻頁： 50 - 57 2010年

Isolation of Microglia Subpopulations 招待有り査読有り

Sawada, M; Suzuki, H

PROTCOLS FOR NEURAL CELL CULTURE, FOURTH EDITION 頁： 231 - 239 2010年

Comparison of [18F]FEPPA and [11C]PBR28, novel peripheral benzodiazepine receptor ligands for PET, in a rat model of neuroinflammation 招待有り査読有り

Toyama, H; Hatano, K; Suzuki, H; Kudo, G; Ichise, M; Wilson, A; Yamada, T; Katada, K; Sawada, M; Ito, K

JOURNAL OF NUCLEAR MEDICINE 50 巻 2009年5月

Protective roles of brain-migrated immature bone marrow cells against NO-dependent neurotoxicity in a brain injury model 招待有り査読有り

Ono Kenji, Yamamoto Naho, Suzuki Hiromi, Sawada Makoto

NEUROSCIENCE RESEARCH 65 巻頁： S43 - S43 2009年

A PRACTICAL PREPARATION OF [18F]FEPPA USING A PROTIC SOLVENT SYSTEM 招待有り査読有り

Hatano, K; Toyama, H; Yamada, T; Kudo, G; Suzuki, H; Ichise, M; Wilson, AA; Sawada, M; Ito, K

JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS 52 巻頁： S273 - S273 2009年

Neuroprotective or neurotoxic phenotypes of activated microglia in neonatal mice in neuronal injuries 招待有り査読有り

Sawada, H; Suzuki, H; Nagatsu, T; Sawada, M

NEUROSCIENCE RESEARCH 65 巻頁： S118 - S118 2009年

Increase in hemokinin-1 mRNA in the spinal cord during the early phase of a neuropathic pain state

MATSUMURA T, SAKAI A, NAGANO M, SAWADA M, SUZUKI H, UMINO M, SUZUKI H

British Journal of Pharmacology 155 巻 ( 5 ) 頁： 767-774 2008年11月

Blockade of microglial glutamate release protects against ischemic brain injury 招待有り査読有り

Takeuchi, H; Jin, S; Suzuki, H; Doi, Y; Liang, J; Kawanokuchi, J; Mizuno, T; Sawada, M; Suzumura, A

EXPERIMENTAL NEUROLOGY 214 巻 ( 1 ) 頁： 144 - 146 2008年11月

Increase in hemokinin-1 mRNA in the spinal cord during the early phase of a neuropathic pain state 招待有り査読有り

Matsumura, T; Sakai, A; Nagano, M; Sawada, M; Suzuki, H; Umino, M; Suzuki, H

BRITISH JOURNAL OF PHARMACOLOGY 155 巻 ( 5 ) 頁： 767 - 774 2008年11月

In vivo imaging of microglial activation using a peripheral benzodiazepine receptor ligand: [(11)C]PK-11195 and animal PET following ethanol injury in rat striatum 査読有り

Toyama Hiroshi, Hatano Kentaro, Suzuki Hiromi, Ichise Masanori, Momosaki Sotaro, Kudo Gen, Ito Fumitaka, Kato Takashi, Yamaguchi Hiroshi, Katada Kazuhiro, Sawada Makoto, Ito Kengo

ANNALS OF NUCLEAR MEDICINE 22 巻 ( 5 ) 頁： 417 - 424 2008年6月

Expression of cytokines and neurotrophins after acute subarachnoid hemorrhage 招待有り査読有り

Sehba, FA; Flores, R; Ono, K; Suzuki, H; Sawada, SM; Kanzawa, T

STROKE 39 巻 ( 2 ) 頁： 650 - 650 2008年2月

Enhancement of glioma formation and growth by brain-migrated immature bone marrow cells 招待有り査読有り

Ono, K; Furukawa, T; Suzuki, H; Sato, E; Sawada, M

NEUROSCIENCE RESEARCH 61 巻頁： S276 - S276 2008年

脳の標的化画像診断-PETによる活性化ミクログリアの分子イメージング- 招待有り査読有り

外山宏, 工藤元, 伊藤文隆, 片田和広, 大橋正男, 中根正人, 籏野健太郎, 加藤隆司, 伊藤健吾, 鈴木弘美, 澤田誠, 市瀬正則

21世紀COE プログラム、超低侵襲標的化診断治療開発センター研究成果報告書頁： 87 - 88 2008年

In-vivo imaging of microglial activation using a novel peripheral benzodiazepine receptor ligand, F-18-FEPPA and animal PET following 6-OHDA injury of the rat striatum; A comparison with C-11-PK11195 招待有り査読有り

Kudo Gen, Toyama H., Hatano K., Suzuki H., Wilson A. A., Ichise M., Ito F., Kato T., Katada K., Sawada M., Ito K.

NEUROIMAGE 41 巻頁： T94 - T94 2008年

動物PETによるラット線状体障害モデルにおけるミクログリア毒性転換の検討招待有り査読有り

鈴木弘美, 外山宏, 籏野健太郎, 工藤元, 伊藤文隆, 小野健治, 加藤隆司, 伊藤健吾, 澤田誠

バイオイメージング 16 巻 ( 2 ) 頁： 93 - 94 2007年10月

N-benzyl-2-(6,8-dichloro-2-(4-chlorophenyl)imidazo[1,2-a]pyridin-3-yl)-N-(6-(7-nitrobenzo[c][1,2,5]oxadiazol-4-ylamino)hexyl)acetamide as a new fluorescent probe for peripheral benzodiazepine receptor and microglial cell visualization. 招待有り査読有り

Laquintana V, Denora N, Lopedota A, Suzuki H, Sawada M, Serra M, Biggio G, Latrofa A, Trapani G, Liso G

Bioconjugate chemistry 18 巻 ( 5 ) 頁： 1397 - 407 2007年9月

Activated microglia affect the nigro-striatal dopamine neurons differently in neonatal and aged mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine 査読有り

Sawada, H; Hishida, R; Hirata, Y; Ono, K; Suzuki, H; Muramatsu, SI; Nakano, I; Nagatsu, T; Sawada, M

JOURNAL OF NEUROSCIENCE RESEARCH 85 巻 ( 8 ) 頁： 1752 - 1761 2007年6月

Neuroprotective effect of exogenous microglia in global brain ischemia. 招待有り査読有り

Imai F, Suzuki H, Oda J, Ninomiya T, Ono K, Sano H, Sawada M

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 27 巻 ( 3 ) 頁： 488 - 500 2007年3月

[Targeting and imaging of brain-specific cell migration]. 招待有り査読有り

Sawada M, Ono K, Suzuki H

Nihon rinsho. Japanese journal of clinical medicine 65 巻 ( 2 ) 頁： 213 - 8 2007年2月

P2-16 新生時由来ミクログリアの活性化がパーキンソン病モデルマウスの黒質ドーパミンニューロンに対して神経保護的にはたらく可能性(脳神経,一般演題,第48回日本組織細胞化学会総会(第8回日中合同組織細胞化学セミナー) 第39回日本臨床分子形態学会総会合同学術集会) 招待有り査読有り

澤田浩秀, 菱田良平, 平田洋子, 小野健治, 鈴木弘美, 村松慎一, 中野今治, 永津俊治, 澤田誠

日本組織細胞化学会総会プログラムおよび抄録集 ( 48 ) 2007年

アルツハイマー病早期診断マーカーのための活性化ミクログリアの画像化-PETによる末梢性ベンゾジアゼピン受容体イメージング- 招待有り査読有り

外山宏, 工藤元, 伊藤文隆, 片田和広, 大橋正男, 中根正人, 籏野健太郎, 加藤隆司, 伊藤健吾, 鈴木弘美, 澤田誠, 市瀬正則

医科学応用研究財団研究報告 26 頁： 415 - 420 2007年

The intra-arterial injection of microglia protects hippocampal CA1 neurons against global ischemia-induced functional deficits in rats 招待有り査読有り

Hayashi, Y; Tomimatsu, Y; Suzuki, H; Yamada, J; Wu, Z; Yao, H; Kagamiishi, Y; Tateishi, N; Sawada, M; Nakanishi, H

NEUROSCIENCE 142 巻 ( 1 ) 頁： 87 - 96 2006年9月

The intra-arterial injection of microglia protects hippocampal CA1 neurons against global ischemia-induced functional deficits in rats

HAYASHI Y, TOMIMATSU Y, SUZUKI H, YAMADA J, WU Z, YAO H, KAGAMIISI Y, TAKEISHI N, SAWADA M, NAKANISHI H

Neuroscience 142 巻 ( 1 ) 頁： 87-96 2006年9月

Modulations of muscle protein metabolism by branched-chain amino acids in normal and muscle-atrophying rats. 招待有り査読有り

Kobayashi H, Kato H, Hirabayashi Y, Murakami H, Suzuki H

The Journal of nutrition 136 巻 ( 1 Suppl ) 頁： 234S - 6S 2006年1月

Activated microglia affect the nigro-striatal dopamine neurons differently in neonatal and aged mice treated with MPTP 招待有り査読有り

Sawada, H; Hishida, R; Hirata, Y; Ono, K; Suzuki, H; Muramatsu, S; Nakano, I; Tsuchida, K; Nagatsu, T; Sawada, M

NEUROSCIENCE RESEARCH 55 巻頁： S201 - S201 2006年

In vivo imaging of microglial activation using a peripheral benzodiazepine receptor ligand, [11C]PK11195 and animal PET following implantation of cultured activated microglia into rat striatum 招待有り査読有り

Kudo, G; Toyama, H; Hatano, K; Suzuki, H; Ichise, M; Ito, F; Kato, T; Sawada, M; Katada, K; Ito, K

NEUROIMAGE 31 巻頁： T148 - T148 2006年

活性型ミクログリアの In Vivo イメージング招待有り査読有り

鈴木弘美, 外山宏, 工藤元, 籏野健太郎, 関亦克彦, 小野健治, 中根正人, 加藤隆司, 伊藤健吾, 澤田誠

バイオイメージング 14 巻 ( 3 ) 頁： 129 - 130 2005年9月

A lentiviral expression system demonstrates that L*protein of Theiler's murine encephalomyelitis virus(TMEV) is essential for virus growth in a murine macrophage-like cell line.

HIMEDA T, OHARA Y, ASAKURA K, KONTANI Y, MURAKAMI M, SUZUKI H, SAWADA M

Virus Research 108 巻 ( 1-2 ) 頁： 23-28 2005年3月

Cytokine production of activated microglia and decrease in neurotrophic factors of neurons in the hippocampus of Lewy body disease brains.

IMAMURA K, HISHIKAWA N, ONO K,SUZUKI H, SAWADA M, NAGATSU T, YOSHIDA M, HASHIZUME Y

Acta Neuropathologica 109 巻 ( 2 ) 頁： 141-150 2005年2月

Cytokine production of activated microglia and decrease in neurotrophic factors of neurons in the hippocampus of Lewy body disease brains 招待有り査読有り

Imamura K, Hishikawa N, Ono K, Suzuki H, Sawada M, Nagatsu T, Yoshida M, Hashizume Y

ACTA NEUROPATHOLOGICA 109 巻 ( 2 ) 頁： 141 - 150 2005年2月

Murine lymph node-derived stromal cells effectively support survival but induce no activation/proliferation of peripheral resting T cells in vitro 招待有り査読有り

Zhou YW, Aritake S, Endharti AT, Wu JH, Hayakawa A, Nakashima I, Suzuki H

IMMUNOLOGY 109 巻 ( 4 ) 頁： 496 - 503 2003年8月

Preservation of hematopoietic properties in transplanted bone marrow cells in the brain. 招待有り査読有り

Ono K, Yoshihara K, Suzuki H, Tanaka KF, Takii T, Onozaki K, Sawada M

Journal of neuroscience research 72 巻 ( 4 ) 頁： 503 - 7 2003年5月

Existence of functional β1- and β2-adrenergic receptors on microglia

Tanaka Kenji F, Kashima Haruo, Suzuki Hiromi, Ono Kenji, Sawada Makoto

Journal of Neuroscience Research 70 巻 ( 2 ) 頁： 232 - 237 2002年10月

記述言語：英語掲載種別：研究論文（学術雑誌）

We examined the expression and function of β-adrenergic receptor (β-AR) subtypes in both isolated primary rat microglia and a rat microglial cell line. RT-PCR analyses revealed that microglia expressed β1- and β2-ARs but not β3-ARs, whereas rat primary peritoneal macrophages expressed only β2-ARs. Stimulation of β-ARs on microglia by norepinephrine (NE) resulted in an increase in the level of intracellular cAMP and the subsequent expression of interleukin-1β mRNA. These effects were prevented by propranolol. Similar results were obtained with other selective β1-AR agonists and antagonists. β2-ARs on microglia were also functional. It is possible that noradrenergic innervations participate in the control of microglial functions via β1-ARs on microglia in the brain, because NE has high affinity for β1- and β3-ARs but little or no affinity for β2-ARs. It seems physiologically significant that microglia can be controlled by NE, which predominates over epinephrine in the brain, whereas macrophages in peripheral tissues can be controlled by epinephrine, which is

DOI： 10.1002/jnr.10399

Web of Science

Modes of activation of mitogen-activated protein kinases and their roles in cepharanthine-induced apoptosis in human leukemia cells 招待有り査読有り

Wu JH, Suzuki H, Akhand AA, Zhou YW, Hossain K, Nakashima I

CELLULAR SIGNALLING 14 巻 ( 6 ) 頁： 509 - 515 2002年6月

Brain-specific migration and protective roles in brain damage of microglia - A new therapeutic approach for catecholamine neuronal disfunctions 査読有り

M Sawada, F Imai, H Suzuki

CATECHOLAMINE RESEARCH: FROM MOLECULAR INSIGHTS TO CLINICAL MEDICINE 53 巻頁： 217 - 220 2002年

Preservation of neurotophin expression in microglia that migrate into the gerbil's brain across the blood-brain barrier.

SUZUKI H, IMAI F, KANNO T, SAWADA M

Neuroscience Letters 312 巻 ( 2 ) 頁： 95-98 2001年10月

Osmotic stress-mediated activation of RET kinases involves intracellular disulfide-bonded dimer formation 招待有り査読有り

Takeda K, Kato M, Wu JH, Iwashita T, Suzuki H, Takahashi M, Nakashima I

ANTIOXIDANTS & REDOX SIGNALING 3 巻 ( 3 ) 頁： 473 - 482 2001年6月

4-hydroxynonenal induces a cellular redox status-related activation of the caspase cascade for apoptotic cell death. 招待有り査読有り

Liu W, Kato M, Akhand AA, Hayakawa A, Suzuki H, Miyata T, Kurokawa K, Hotta Y, Ishikawa N, Nakashima I

Journal of cell science 113 ( Pt 4) 巻頁： 635 - 41 2000年2月

Molecular Mechanism of Activation and Superactivation of Ret Tyrosine Kinases by Ultraviolet Light Irradiation 招待有り査読有り

Kato Masashi, Iwashita Toshihide, Akhand Anwarul A., Liu Wei, Takeda Kozue, Takeuchi Kei, Yoshihara Motoi, Hossain Khaled, Wu Jianghong, Du Jun, Oh Chanho, Kawamoto Yoshiyuki, Suzuki Haruhiko, Takahashi Masahide, Nakashima Izumi

ANTIOXIDANTS & REDOX SIGNALING 2 巻 ( 4 ) 頁： 841 - 850 2000年

Normal regulatory alpha/beta T cells effectively eliminate abnormally activated T cells lacking the interleukin 2 receptor beta in vivo 招待有り査読有り

Suzuki H, Zhou YW, Kato M, Mak TW, Nakashima I

JOURNAL OF EXPERIMENTAL MEDICINE 190 巻 ( 11 ) 頁： 1561 - 1571 1999年12月

Exogenous microglia enter the brain and migrate into ischaemic hippocampal lesions.

IMAI F, SAWADA M, SUZUKI H, ZLOKOVIC BV, KOJIMA J, KUNO S, NAGATSU T, NITATORI T, UCHIYAMA Y, KANNNO T

Neuroscience Letters 272 巻 ( 2 ) 頁： 127-130 1999年9月

Exogenous microglia enter the brain and migrate into ischaemic hippocampal lesions

F Imai, M Sawada, H Suzuki, BV Zlokovic, J Kojima, S Kuno, T Nagatsu, T Nitatori, Y Uchiyama, T Kanno

NEUROSCIENCE LETTERS 272 巻 ( 2 ) 頁： 127 - 130 1999年9月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：ELSEVIER SCI IRELAND LTD

We compared migration of systemically injected microglia into normal brain vs. ischaemic brain using a model of ischaemic hippocampal lesion. Microglia were labeled by a fluorescent dye using our standard phagocytosis procedure of microscopic particles and then injected intra-arterially into Mongolian gerbils subjected to ischaemia reperfusion neuronal injury. Delayed death of pyramidal neurons was confirmed by conventional histological analysis and dUTP nick end labeling (TUNEL) method. Clusters of dye-tagged cells migrating into the hippocampal ischaemic lesions were confirmed histochemically to be microglia. Since peripherally injected microglia exhibit specific affinity for ischaemic brain lesions and does not exacerbate ischaemic neuronal injury in the present model, we suggest that microglia may have a potential to be used as a piggy-back ride to deliver therapeutic genes and/or drugs for CNS repair following transitory global ischaemic insult. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.

DOI： 10.1016/S0304-3940(99)00592-3

Web of Science

PubMed

Brain-specific gene expression by immortalized microglia cell-mediated gene transfer in the mammalian brain

SAWADA M, IMAI F, SUZUKI H. HAYAKAWA M, KANNO T, NAGATSU T

FEBS Letters 433 巻 ( 1-2 ) 頁： 37-40 1998年8月

Migration activity of microglia and macrophages into rat brain.

IMAI F, SAWADA M, SUZUKI H, KIYA N, HAYAKAWA M,NAGATSU T, MARUNOUCHI T, KANNO T

Neuroscience Letters 237 巻 ( 1 ) 頁： 49-52 1997年11月

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